AIDS MD Heinrich Kremer - thiol deficiency

[Guest guest]

Here is detail to support what I have been saying for years about real

AIDS, not HIV+

test status, being the condition of an immune system which has lost its

civility by

losing its cellular immune response, and having been misled into a

police-state

witch-hunt hysteria in the form of a reliance on antibody response, what

this

author describes as gas warfare, and prescribed drugs and chemotherapy,

which

only accelerate a descent into illness and death. The ignorant

police-state immune

system which has lost its civility, its cellular immune response, is a

witch-hunt

because cells that could be healed by cellular immune response are

thought-crimed

and killed by an inquisition, and because the police-state allergy

auto-immune

system is agency of the chemical companies that mark cells for

guilt-by-association,

and the police state immune system obtains chemical weapons which are

tactically

efficient but strategically inefficient(ultimately lethal), and finally,

that the police

state immune system forms provocateur cells to justify further abuses.

The DTH test debunks the notion that low t-cell counts(unscientifically

assumed to

be caused by HIV), equate to acquired immune deficiency syndrome(AIDS). Four

weeks after Heinrich Kremer pointed out this implication of the DTH

test, that

patented test was withdrawn from the market by the patent-holder, in

violation

of contracts, as accessory and accomplice to intentional global genocide.

" Within any fit population 5% report anyway T4 cell values below 500 per

microliter in

their blood stream...In fit persons the T4 cell values can drop even

below 200 per microliter

without a serious loss of cellular immunity functions "

" For patients tested HIV positive, this T4 cell level is already

interpreted as reason for a

chemo-therapeutical and chemo-antibiotic intervention through HIV/AIDS

therapy...

Valid information can be obtained through the DTH recall antigen test

(antigen recall test

of the skin, delayed type hypersensibility. "

" (*Note*: Four weeks after publication of this book (in November 2001),

the DTH test was

withdrawn from circulation worldwide by its producer, the pharmaceutical

industrial group

Aventis-Mérieux (which includes the subsidiary Mérieux-Pasteur). As

Aventis-Mérieux (now

merged with French pharmaceutical group Sanofi) is the patented monopole

holder of the

DTH test, there's no alternative diagnostic instrument. Biosyn, the

German DTH test vendor,

pointed out in a written statement, that Aventis-Mérieux had for no

apparent reason abruptly

stopped delivering the DTH test (including the last charge, contrary to

contract). They, Biosyn,

had been trying to get a licence for the production of the DTH test by

themselves, but Aventis-

Mérieux chose to prevent their attempt. This behaviour can only be

understood on the obvious

background, that Aventis-Mérieux has at that time (November 2001), been

involved in studies

using the so-called naked DNA as " anti HIV vaccine " on human

experimental subjects in

Uganda and Thailand. Such vaccination was thought of as promising

billions of dollars sales. "

" An easy-to-handle DTH test could be detrimental to this purpose. As,

for example, in African

countries, the so-called anti-HIV-antibody test frequently reacts

positive for persons previously

infected with tuberculosis or malaria pathogens, which show an endemic

occurrence there.

Conventional scientists in addition deny any connections of this

reaction with a so-called HIV

infection. In such cases, the use of DTH skin reaction tests would show

a sufficient T1 immune

cell reaction, if subjects of the test didn't manifest chronically

present TB or malaria exposure

of clinical relevance. A routine-use of a DTH test before a

mass-vaccination with so-called naked

DNA would consequently have been able to unmask the global so-called HIV

infection as a

scientific disinformation campaign. In the meantime, probation

experiments with so-called naked

DNA against so-called HIV infection have been suspended. Only after

leukaemia appeared in

infants, treated with genetically upgraded stem cells, to fight a

serious immune deficiency, a

global moratorium for gene therapy human trials has been declared "

[the following not for HIV+ test result people, but for real AIDS as

indicated by not taking

HIV drugs, prednisone, cortisone, or antibiotics, but even so

experiencing symptoms such as

cancer and pneumonia and thrush, possibly confirmed by DTH test if that

became available

again. also valuable as component of treatment for intestinal problems

and in mercury

amalgam filling detox after amalgam removal--thus relevent to " MS " if

mercury induced]

" compensation of the thiol deficiency "

" The pathognomic symptom of cellular immune deficiency(AIDS) and other

systemic diseases

is lack of cysteine and glutathione. (Herzenberg 1997, Dröge 1997 b,

1998, Hässig 1998

d, Kremer 1999)...for 2 to 4 weeks at the beginning of the

biological-compensatory therapy at

least 2 grams of glutathione and 5 to 10 grams of N-acetyle-cysteine

must be orally administered

per day...cysteine treatment should be continued for another six months

with a daily dosage of

5 to 10 grams of N-acetyl-cysteine. Cysteine and methionin, the later is

converted in the liver to

cysteine, can be taken in addition as part of daily nutrition. It is

contained in low fat curd cheese

and other native organic dairy products (Bounous 1993). Due to the

deficit of convertible protons,

thiol deficiency causes a glutamine decrease with exaggerated protein

reduction in the skeletal

muscles (loss of body weight, wasting syndrome). The oral intake of up

to 40 grams/day of high

dosage glutamine can retune the synergic effect between glutamine and

cysteine levels for the

helper T cells maturation (Shabert 1999)...Simultaneously this effect

improves the regeneration

of intestinal and lung mucous membranes, energy metabolism of the cell

symbioses and acid-base

balancing...The glutamine facilitates detoxification activity in the

liver via the glutathione system;

it slows down the urea production due to decrease in the arginine

splitting in urea and ornithine.

If in case of a clear arginine deficit and the resulting lack of NO gas

production (as part of pre-AIDS

and AIDS), the thiol and glutamine balance is complimented by doses of

up to 30 grams of arginine

per day and up to 2% of the caloric intake respectively. By this the

cellular immune performance

(T4 help cells, natural killer cells, neutrophilic granulocytes) can be

augmented significantly

(Barbul1990, Bower 1990). "

" garlic, onions, broccoli, cabbage species and algae, micro-algae,

omega-3, coenzyme Q10,

alpha-lipoic, l-carnitine, B "

" Vitamin E and vitamin C generate radical chain reactions as

intermediate states, which must be

compensated for by the glutathione system (Ohlenschläger 1994),

therefore a given thiol deficiency

can be AGGRAVATED by the intake of a high dosages of those vitamins. "

-Bob

Felix de Fries wrote:

> *Study group AIDS-therapy*

>

> c/o Felix A. de Fries

>

> Eglistr. 7 CH-8004 Zürich

>

> Tel./Fay:0041 1 401 34 24

>

> felix.defries@... <mailto:felix.defries@...>

>

> Zurich, 7^th November 2004

>

>

>

> To those affected and their doctors

>

> To institutions and

>

> to media world wide

>

>

>

>

>

> AIDS-therapy: *MD Heinrich Kremer: " The Life Saving Knowledge of Healing " *

>

>

>

> Dear Sir / Madam

>

>

>

> The world's powerlessness against AIDS has once more time been

> demonstarted at the Bangkok world AIDS conference:

>

> - the number of persons testet HIV positive are

> still increasing,

>

> - ongoing trials with HIV vaccines must be considered as failed,

>

> - antiviral combination therapy can't be a solution for AIDS as

> it effects severe damage to the organism.

>

>

>

> In Bangkok once more the HIV-retro virus was seen as the only cause

> for the many and varied illnesses defining the AIDS-Syndrom. Again,

> other aspects such as repeated infection (i.e. with polluted water),

> malnutrition, poor living conditions, toxins in the evironment, abuse

> of antibiotics and adverse effects of antibiotics and vaccines were

> not brought forth for discussion at this years World-AIDS- Conference.

>

>

>

> For now more than 20 years, scientists worldwide have investigated

> such causes leading to the epidemic spread of the diseases, that

> define the AIDS-syndrome.

>

>

>

> In his book, " A Silent Revolution in Cancer- and AIDS- Therapy " (which

> is not jet available in English) MD Heinrich Kremer has compiled all

> their knowledge. On the basis of fundamental nineties research on

> nitric oxide and cancer, he arranged this information in a entirely

> new context of comprehension. In the book's chapter on therapy he

> demonstartes the means and remedies of a holistic treatment of AIDS,

> which have been proven to be effective in scientific studies over the

> last 10 years.

>

>

>

> We have translated part of this chapter into English for your

> convenience. In the attachments you also find the index and the

> bibliography of this book and Kremer's latest article on antiviral

> AIDS-therapy, in which he analyses the labor methods used for the

> postulation of the HIV-retroviruses and the effects of the

> antiretroviral treatment.

>

>

>

> We wish You an imformative read

>

>

>

> AIDS therapy Study group

>

> Felix de Fries

>

>

> *Dr. med. Heinrich Kremer: A silent revolution in cancer and AIDS

> therapy*

>

> * *

>

> *New research results concerning the factual causes of disease and

> death confirm the effectiveness of a therapy based on biological

> compensation.*

>

>

>

> German Edition: Heinrich Kremer: Die stille Revolution der Krebs- und

> AIDS-Therapie Ehlers Verlag Wolfratshausen 2001 www.ehlersverlag.de

> <http://www.ehlersverlag.de/> price: EUR 50.-

>

> 535 pages, 17 charts, ISBN

> 3-934196-20-9

>

>

>

> Excerpt from chapter XI: Page 416-443

>

> * *

>

> * " The Life saving knowledge on healing " *

>

> * *

>

> *On diagnostics, prophylaxis and applied therapy to AIDS and other

> systemic diseases - _balance instead of elimination_*

>

>

>

> (Excerpts on this webpage are published with author's permission)

>

>

>

> Disposition factors can be epidemiologically justified. They also

> explain why the pathogenetic distribution patterns manifest in a

> Gaussian distribution curve, equally for excessive expositions as in

> collective populations and differing risk groups.

>

>

>

> While the majority of the exposed individuals will maintain a variable

> redox balance with flexible cytokine patterns, a minor percentage

> will develop a distinct type-I overreaction resp. a distinct type-II

> counterreaction. To presume a fatal mass-infection transmissible to

> everybody, ending in inevitable death was a priori a medical

> construction beyond a biological-evolutionary reality.

>

>

>

> In the case of the so-called HIV-induced AIDS, it seamed particularly

> questionable to presume that the humoral (antibody-supported) immunity

> was operating successfully (Mildvan 1982) while the cellular immunity

> of the T4 helper cells against intracellular germs failed, so

> opportunistic infections could develop.

>

> Only once patients were treated with AZT chemotherapy massive

> bacterial infections happened as a matter of consequence of maturation

> inhibition of bone marrow cells (Rosenthal 1994), (Marco 1998, 1998).

>

>

>

> Because the evolutionary and biologically programmed coaction of

> exposition and disposition factors has not been sufficiently

> understood, HIV/AIDS medicine provoked the appearance of combined

> acquired cellular and humoral immune deficiency SCID (for severe

> combined immunodeficiency) by prescribing chemotherapeutics on the

> basis of the objectively incorrect theory that " HIV causes AIDS " . The

> clinical and epidemiologic results demonstrate with abundant clarity

> the deficits of modern medicine, resulting from underestimating toxic

> and pharmaco-toxic stressors and of the one-sided fixation on outdated

> 19^th century infection theories with sophisticated 20^th century

> biotechnological methods.

>

>

>

> The HIV and AIDS establishment's massive projection of a supposed

> pandemia (mortal infection spreading on whole populations) reveals

> that in the case of doubtless increased collective charging with

> immune stressors (endemic multi-infectiosity, contaminated drinking

> water, undernourishment, adverse general life conditions et al.),

> special disposition factors must supervene when triggering acquired

> immunodeficiency.

>

>

>

> Professor Duesberg, retrovirus cancer scientist and molecular

> biologist at Berkeley, California, one of the most severe critics of

> the " HIV causes AIDS " theory, considers the so-called HI virus to be a

> " passenger virus " . He regards toxic reasons like excessive consume of

> illegal drugs, nitritinhalation as sexual doping agent, medical

> chemotherapy and also the injection of highly contaminated clotting

> protein factors against hemophilia as the real causes of AIDS. On the

> occasion of Pretoria specialist's conference on July 2000 he stated:

>

> " In the light of this hypothesis the new epidemic of HIV-antibodies

> would simply reflect a new epidemic of HIV-antibody testing,

> introduced and inspired by new American biotechnology. This technology

> was developed during the last 20 years for basic research to detect

> the equivalents of biological needles in a haystack, but not to

> " detect " the massive invasions of viruses that are necessary to cause

> ALL conventional viral diseases (Duesberg, 1992; Duesberg & Schwartz,

> 1992; Duesberg, 1996; Mullis, 1996; Duesberg & Rasnick, 1998; Mullis,

> 1998). But this technology is now faithfully but inappropriately used

> by thousands of AIDS virus researchers and activists to detect latent,

> ie. biochemically and biologically inactive HIV or even just

> antibodies against it (Duesberg & Bialy, 1996)! The same technology

> also provides job security for other virologists and doctors searching

> for latent, and thus biologically inactive, viruses as their preferred

> causes of Kaposi's sarcoma, cervical cancer, leukemia, liver cancer,

> and rare neurological diseases - without ever producing any public

> health benefits (Duesberg & Schwartz, 1992)...

>

> To all of us who have been subjected to the American AIDS rhetoric,

> and indeed the rhetoric of our first meeting in Pretoria last May,

> about the " catastrophic dimensions " of African AIDS (Washington Post,

> April 30, 2000), the healthy African growth rates come as a big

> surprise. Take as an example of this rhetoric President Clinton's

> recent designation of AIDS as a " threat to US national security ...

> spurred by US intelligence reports that looked at the pandemic's

> broadest consequences, ... particularly Africa ... [and] projected

> that a quarter of southern Africa's population is likely to die of

> AIDS ...(Washington Post, April 30, 2000). The alarming tone of WHO's

> joint United Nations Programme on HIV/AIDS, " AIDS epidemic update:

> December 1999 " (UNAIDS December 1999), announcing that Africa had

> gained 23 million " living with HIV/AIDS " , because they are " estimated "

> carriers of antibodies against HIV, since the " early 80s " (WHO, Weekly

> Epidemiological Record 73, 373-380, 1998) is equally surprising in

> view of information available to the agency. Neither the WHO nor the

> United Nations point out that Africa had gained 147 million people

> during the same time in which the continent was said to suffer from a

> new AIDS epidemic.

>

> Likewise, South Africa has grown from 17 million to 37 million in 1990

> (United Nations Environment Programme, June 15, 2000), and to 44

> million now ( " HIV/AIDS in the Developing World " , U.S. Agency for

> International Development & U.S. Census Bureau, May 1999). In the last

> decade South Africa has also gained 4 million HIV-positive people (A.

> Kinghorn & M. Steinberg, South African Department of Health, undated

> document probably from 1998, provided at the Pretoria meeting). Thus

> South Africa has gained 4 million HIV-positives during the same decade

> in which it grew by 7 million people. Moreover, although the 23

> million " estimated " HIV-antibody positives are said to be " living with

> HIV/AIDS " by the WHO, the agency does not offer any evidence for

> morbidity or mortality exceeding the modest numbers, ie. about 75,000

> cases annually, reported by the it's Weekly Epidemiological Records

> (0,012% of Africa's whole population) (WHO Weekly Epidemiological

> Records 73,373-380, 1998).

>

> The agency's estimates of HIV-positives are indeed just " estimates " ,

> because according to the 1985-Bangui definition of African AIDS as

> well as to the current " Anonymous AIDS Notification " forms of the

> South African Department of Health - no HIV tests are required for an

> AIDS diagnosis (Widy-Wirski et al., 1988; Fiala, 1998).

>

> In addition the WHO promotes the impression of a microbial AIDS

> epidemic, by reporting African AIDS cases cumulatively rather than

> annually (WHO's Weekly Epidemiological Records since the beginning of

> the epidemic). This practice creates the deceptive impression of an

> ever growing, almost exponential epidemic, even if the annual

> incidence declines (Fiala, 1998).

>

> It would follow that the estimated increases in African HIV antibody

> (!)-positives do not correlate with decreases in any African

> population. On the contrary, they correlate with unprecedented

> simultaneous increases in the country's populations - hardly the

> " catastrophe " imagined by the Washington Post and propagated by the

> WHO and the American AIDS establishment. But this deceptive AIDS

> propaganda biases a scientific analysis of African AIDS by all those

> who are not aware of the facts " (Duesberg 2000).

>

>

>

> In other words, the actual data recorded in the WHO epidemiological

> reports total morbidity and death rates in African states to be hardly

> higher than in western countries. Namely 0.012% of Africa's total

> population fall ill and die of AIDS per year (WHO Weekly

> Epidemiological reports since 1991), compared to 0.001 to 0.002% of

> total populations in western countries (CDC 1999, Koch

> Institute 1999).

>

> The absurd propagandistic claims insisting on a " African pandemic "

> distributed to the international media by the WHO are based on

> arbitrary extrapolation of small random samples received by abusing

> " American biotechnology " , using the so-called anti HIV antibody test

> (Duesberg 2000).

>

>

>

> Based on the not very reliable acquisition of pathogen data, compared

> to western countries and because of the small fund of medical research

> results in developing countries, it is much less obvious to draw

> conclusions on the exposition and disposition interaction for

> morbidity and mortality in causal connection with typeII cell

> dyssymbioses' systemic diseases.

>

> However the population explosion data in African countries shows

> comparability with demographic processes in western countries 150

> years ago. Infectious disease rates will be reclining and toxic stress

> will be increasing with gradual improvement of general life conditions

> and of medical and social standards.

>

>

>

> Increased sex-unrelated collective charge with variegated

> immunostressors with simultaneously " surprising " (Duesberg 2000) low

> AIDS incidence (WHO Weekly Epidemiological Records since 1991) when

> compared to Western countries and the parallel population explosion in

> Africa give reason to presume that disposition factors must play a role.

>

> Consequences for developing countries as for the western countries are

> the same: protection from the abuse of " American biotechnology "

> (Duesberg 2000) and the " blessings " of western chemotherapy and

> chemoantibiotics while promoting knowledge on evolutionary

> biologically programmed redox protection.

>

>

>

> Disposition factors act over the peroxidation control system (creation

> of hydrogen peroxides, H_2 O_2 and lipoxides) and nitrosylation of

> transcription proteins (bonding NO and NO derivatives with hydrogen

> sulphide groups of proteins containing cysteine, RSNO).

>

> In the case of too high glutathione consumption this control system

> initially rises, as a sensor, the antioxidative gene's activity and

> the H_2 O_2 ,lipide peroxidation and RSNO metabolisation (Hausladen

> 1996).

>

>

>

> After the glutathione and other antioxidative enzymes (katalase,

> superoxid-dismutase, selenium dependent glutathione peroxidase,

> glutathione transferases, NADH dependent glutathione

> reductase)neosynthesis depletion, the hypoxic/pseudo-hypoxic emergency

> routine will be switched on.

>

>

>

> The early and sustained switch of the cytokine balance to humoral and

> antibody-supported immune response was, under evolutionary biological

> aspects advantageous, because the bacterial threat predominant in the

> course of the evolution could be efficiently averted.

>

> Bacteria proliferate faster than opportunistic pathogens. They can be

> inhibited and destroyed efficiently, through the defence mechanisms

> of non-cell-related humoral immunity, complement formation,

> opsonisation (coating of bacteria membranes by special target

> molecules for antibodies) and of the antibodies themselves, which are

> formed by B-lymphocytes maturated in the bone marrow.

>

> Larger mycosis pathogens and parasites, equipped with mitochondria,

> and mycobacteria provided with a special cell membrane are stopped

> most efficiently by the non-specific and specific immune cell network

> co-action.

>

> If not inhibited in time by the gas attack, many parasites can

> invalidate the NO gas synthesis by special surface molecules

> (glycosinositole phospholipids).

>

> Multicellular (extracellular) parasites can emit specialized

> histodestructive proteins (proteinases), which trigger a type2

> cytokine response (TH2 immune response)as adequate reaction, since

> combating worms for example would need too large quantity of NO gas

> which would in turn damage the patient's own tissue cells.

>

>

>

> Metastatic cancer cells also utilize the biochemical initialization of

> proteinases for pervading tissue and deactivate the NO gas production

> in neighboured cells.

>

> Characteristic for cancer cells is their abased gas production

> (Ignarro 2000) and extreme irritability to high NO gas levels to

> them(Xie 1996, Chinje 1997).

>

> In the net result a one-sided TH2 (cytokine2) immune response is an

> adversarial disposition for blocking intracellular pathogens (fungi,

> parasites, mycobacterias, some virus species) and metastatic cancer

> cells (Zvibel 1993, Liew 1994, 1995a, 1995b, Mosmann 1996, Abbas 1996,

> Lucey 1996, Xie 1996).Thus, all depends on an appropriate and flexible

> combination of a defence and regulation strategy. The change of the

> relevance of the evolutionary advantage of the redox sensitive lasting

> type2 cytokine immune response while toxic and pharmacotoxic effects

> as an impact of civilization as a net result of civilizing progress

> and of development of modern medicine, especially through the

> introduction of vaccination programs and antibiotics over the last 50

> years, have gained in importance.

>

>

>

> Persons with a particularly high redox sensitive disposition are at a

> disadvantage because they respond to toxic influences faster and with

> an exaggerated type-II counterreaction in the manner normally suited

> for inhibiting extracellular bacteria or multicellular parasites.

>

> Thus, the immune system chooses the evolutionary biological

> programmed, but " wrong " strategy, because it is mislead by toxic

> stressors which didn't exist as part of natural evolution.

>

>

>

> This development is reflected in the steady rise of cancer and other

> systemic diseases over the last 100 years in the developed countries.

>

> The quintessential source of toxic exposition which favour cancer and

> other systemic diseases development in the industrialized countries,

> are today: toxin residues in nutrition, in environment and at working

> places, and the use of tobacco (Loeppky 1994, 1998, Waite 1998,

> North 1998) as well as pharmacotoxic medication and pharmaceutics

> toxic decomposition products..

>

> The individually disposed efficiency of redox depending detoxification

> capacity is the critical disease factor for the actual incidence of

> type-II cell dyssymbioses through toxic and pharmaco-toxic nitrosation

> and peroxidation.

>

>

>

> On occasion of the nobel prize laureate conference held in u on

> Lake Constance in 1967 Warburg made his historic declaration: that

> there is no disease whose prime cause is better known than cancer

> (Warburg 1967). Since then an expanding field of research has been

> established dealing with an individual disposition for metabolism

> processes on the detoxification of medicaments in the human organism.

>

>

>

> This field of research has very quickly been expanded on direct and

> indirect effects of toxic substances on cancer genesis (overview:

> Kalow 1993, Daly 1994).

>

> These studies concentrate, according to the molecular genetics

> mainstream of cancer research, on the variability of genetic

> expression for biosynthesis of detoxification through enzyme-proteins

> (genetical enzyme polymorphism):

>

> The paradigm of cancerogenic chemical products' mechanisms of

> application is well established in a cell culture model and in animal

> systems.

>

>

>

> Studies on human beings seem to support the possibility that most

> cancer forms can be triggered through contacts with chemicals and

> nutrition and that they progress through various forerunner stages of

> tumorogenic tissue damage consisting of partially transformed cells to

> fully developed metastatic cancer cells (Vogelstein 1993).

>

>

>

> The progression stadium can be increased in rat models through

> treatment with not necessarily carcinogenic, tumour promoting

> substances (Hennings 1993).

>

> Fixing the mutation in the genome, those chemicals are to be

> visualized as intermediaries for cell proliferation.

>

> Another class of chemicals called non-genotoxic carcinogens was

> described in rat model systems ( 1993, Barret 1995, Costa 1995).

>

> These substances are not activated as genotoxic descendants in

> metabolism but presumably alter cell division cycle control. Many

> non-genotoxic carcinogenics are also tumour promoters, but their

> mechanisms of action are not yet known.

>

>

>

> The concept persists that humans differ in their sensitivity to

> cancer. Certain individuals can be more sensitive while others are

> more cancer resistant. This may be due to a number of factors

> including: state of health, nutritional condition and gender.

> Considering all known facts concerning the mechanisms of carcinogens,

> the general presumption is, that genetic background could play an

> important role. Obvious candidates complying with such a theory are

> genes which activate the coding for the enzymes ( 1995, Nebert

> 1996). Such enzymes' variable quantities of expression can result from

> a increased or lowered activation of carcinogens. It is indeed well

> established that genetic differences appear during the detoxification

> expression of enzymes (Hirvonen 1999). Re-foetalized tumour cells can

> appear time-depending (type-II counterreaction of cell dyssymbiosis).

>

>

>

> Working with prooxidative chemotherapeutics in a part of the cells

> this situation allows for selective forcing of the desired

> apoptosis/necrosis on one hand (type-I cell symbiosis overregulation),

> but on the other hand this can also accelerate a fully developed

> transformation into metastatic cancer cells inside other cells. In

> primary tumour tissue, and also secondary in different tissues all

> phases of the yet compensated cell dyssymbiosis, can switch over

> unpredictably into a decompensated cell dyssymbiosis stadia.

>

>

>

> It is characteristic for the chemotherapeutical treatment principle

> that patients with a particularly increased redox sensitivity

> disposition, who fell ill because of this genetically and

> supragenetically disposed redox sensitivity, will not only have exact

> cell dyssymbioses in manifest tumour tissue but also in other tissue

> types and that tumour cells will respond to the chemotherapeutic

> target attack in manifest decompensated tissue in different manners in

> different stadia.

>

> Therefore only a conditional homogenic responsiveness of tumour cells

> to chemo-therapeutics can be assumed, and the results of therapy

> schemata can not be sufficiently calculated individually. For patients

> with a systemic disease consequently, the distinctive genetic

> polymorphism of carcinogen-activating detoxifying enzymes manifest in

> the disease's course.

>

>

>

>

>

> Redox sensitive variability of detoxification enzymes applies mainly

> cytochrome P450-dependent and flavin-containing monoxygenases, epoxide

> hydralases, glutathione transferases, N-acetyl transferases.

> NAD(P)H-ubiquinone oxidoreductases, myeloperoxidases and others

> (overview: Wilkinson 1997, Hirvonen 1999).

>

> Such patients depend most urgently immediately on a balancing of the

> thiol pool and redox state. Chemotherapeutical treatment and the

> consequent extreme prooxidative stress must inevitably have a

> counterproductive effect, because such a therapy is done normally

> without compensating thiol pool depletion. Chemotherapy triggers the

> desired destructive cell effects as well as individually non

> calculable cell dyssymbiotic counterreactions, causing among other

> things systemic wasting syndrome.

>

>

>

> If resulting in questionable conclusions genetic tests have been

> developed to determine individually disposed variability of

> detoxification enzymes' isoforms. In the USA for example, prophylactic

> mastectomies are being performed to avoid breast-cancer.

>

> Such deterministic prognostics by means of genetic tests are for

> different reasons to be assessed most critically. As far as they are

> significant at all, they could only give reason as targeted influence

> on an exposition-disposition interaction via nutrition measures and

> individual balance and regulation therapy.

>

>

>

> " Evidently to determine possible risk genome types for metabolism

> processes rapid progress in methodology must take place. This progress

> includes if minimally so invasive methods for extracting test probes

> (for example cells from oral mucosa or cell probes from urine),

> automatic DNA extraction in combination with processing probes by

> robots and genetic test methods based on specialized analysis of

> oligonucleotids.

>

> At present, many research laboratories perform associated-studies, and

> contradictory reports appear in technical literature. There are

> different sources for false interpretations which partially explain

> the opposing statements, initially it's small studies which show a

> positive association. This results in the significant problems to gage

> their importance when calculating the planning of follow-up studies.

>

> Public reports about results with a high association profile (between

> gene aberrances and cancer incidence), turn eventually out to be

> false, and therefore are equally problematic.

>

> Furthermore, recently discussions assessing one-sided information have

> taken place - the selective publication of only positive associations.

>

> If the above mentioned, potentially false interpretations can be

> meticulously controlled, genetic triage studies can become more

> helpful in the near future for identifying susceptible persons and

> population subgroups exposed to environmental toxins.

>

> Genetic technology enterprises offer genetic tests to companies and to

> individuals. As long as these methods are not scientifically and

> ethically beyond any possibility of doubt, they can profit only the

> manufacturing firms selling the tests. There exists a need to raise

> important ethic questions concerning the social consequences for our

> public health care " (Hirvonen 1999).

>

>

>

> This gene-technological development of tests demonstrates the

> predominant tendency to overemphasize structural gene aberrations

> instead of considering the bioenergetic conditions for genetic

> expression for biosyntheses of enzyme proteins and studying exposition

> risks and tackle individual dispositions by non-aggressive prevention.

>

>

>

> The entirety of all available experimental, clinical and

> epidemiological data make it necessary to consider in clinical

> practice more acting-directing principles of diagnostics, prophylaxis

> and therapy of systemic diseases. Because of their relative

> straightforwardness of their cause-and-effect ratio between exposing

> and disposing factors, Pre-AIDS and AIDS present a good model

> describing the overregulation and counterregulation of the cell

> symbiotic interactions in immune and non-immune cells and the

> consequential systemic processes.

>

>

>

> There's no cause for panic should a patient find himself stigmatized

> as " HIV positive " as a result of the so-called HIV test. Any such

> death prognosis are rather an expression of limited medical knowledge

> than justified in biological fact. The period of incubation from the

> so-called HIV sero-conversion to manifest symptoms averages 12 - 15 years.

>

> In the USA, where patients are treated aggressively and early with

> prooxidative chemotherapeutics about 5% of patients stigmatized as HIV

> positive fall ill.

>

> Consequently, it would take for all so-called HIV positives 20 years

> to actually fall ill.

>

> However the factual incidence depends on the persistence of primary

> exposition risks, on secondary exposition risk through aggressive

> therapy schemata and the refraining from systematic compensatory and

> regulatory therapy, if necessary at all.

>

> Rather than merely concluding the patient belongs to a risk group,

> first and foremost a careful anamnesis would be called for.

>

>

>

> Allergy predisposition or atopic skin diseases, asthma etc. can be

> important indicators for a patient's disposition for

> type-2-cytokine-reactions and increased antibody production.

>

> The absence of typical bacterial children's diseases can, with other

> indicators, also be a sign for a type-2-disposition.

>

>

>

> More than 70 symptomatic conditions can result in a positive HIV test

> reaction. Hence even HIV/AIDS medical treatment categorizes 5% of all

> so-called positive HIV tests as a priori insignificant diagnostic

> findings. Therefore, medical care can not and must not be guided by

> the positive result of any so-called HIV test, unless an actual immune

> deficiency virus " HIV " has been educed.

>

>

>

> Taken on it own, the number of differentiated cells measured within

> the immune cell network and the immune globulin classes, can not be

> considered a reliable indicator for the actual existence of an immune

> cell deficiency in symptom free patients. Within any fit population 5%

> report anyway T4 cell values below 500 per microliter in their blood

> stream.

>

>

>

> For patients tested HIV positive, this T4 cell level is already

> interpreted as reason for a chemo-therapeutical and chemo-antibiotic

> intervention through HIV/AIDS therapy

>

> In fit persons the T4 cell values can drop even below 200 per

> microliter without a serious loss of cellular immunity functions.

> Without seriously limiting their functionality, the number of helper T

> immune cells in the blood stream depends on multiple influences.

>

> Valid information can be obtained through the DTH recall antigen test

> (antigen recall test of the skin, delayed type hypersensibility.

>

>

>

> (*Note*: Four weeks after publication of this book (in November 2001),

> the DTH test was withdrawn from circulation worldwide by its producer,

> the pharmaceutical industrial group Aventis-Mérieux (which includes

> the subsidiary Mérieux-Pasteur). As Aventis-Mérieux (now merged with

> French pharmaceutical group Sanofi) is the patented monopole holder of

> the DTH test, there's no alternative diagnostic instrument. Biosyn,

> the German DTH test vendor, pointed out in a written statement, that

> Aventis-Mérieux had for no apparent reason abruptly stopped delivering

> the DTH test (including the last charge, contrary to contract). They,

> Biosyn, had been trying to get a licence for the production of the DTH

> test by themselves, but Aventis-Mérieux chose to prevent their

> attempt. This behaviour can only be understood on the obvious

> background, that Aventis-Mérieux has at that time (November 2001),

> been involved in studies using the so-called naked DNA as " anti HIV

> vaccine " on human experimental subjects in Uganda and Thailand. Such

> vaccination was thought of as promising billions of dollars sales.

>

>

>

> An easy-to-handle DTH test could be detrimental to this purpose. As,

> for example, in African countries, the so-called anti-HIV-antibody

> test frequently reacts positive for persons previously infected with

> tuberculosis or malaria pathogens, which show an endemic occurrence

> there. Conventional scientists in addition deny any connections of

> this reaction with a so-called HIV infection. In such cases, the use

> of DTH skin reaction tests would show a sufficient T1 immune cell

> reaction, if subjects of the test didn't manifest chronically present

> TB or malaria exposure of clinical relevance.

>

> A routine-use of a DTH test before a mass-vaccination with so-called

> naked DNA would consequently have been able to unmask the global

> so-called HIV infection as a scientific disinformation campaign. In

> the meantime, probation experiments with so-called naked DNA against

> so-called HIV infection have been suspended. Only after leukaemia

> appeared in infants, treated with genetically upgraded stem cells, to

> fight a serious immune deficiency, a global moratorium for gene

> therapy human trials has been declared.)

>

>

>

> For the actual functionality of type-1 cytokines, activating a

> cytostatic NO-defence-gas against the intracellular pathogens after

> antigen stimulation, a strong DTH test reaction has to be considered a

> reliable indicator (Christou 1986, 1995, Mosmann 1989, Hässig 1998b).

>

> Therefore, the actual danger of intracellular opportunistic infections

> is not given only due to the positive result of a so-called HIV test.

>

>

>

> A weak or anergic (ineffective) DTH skin test reaction indicates the

> probability of a prevalent shift to type2 cytokine state and the

> endangering for opportunistic infections. To measure the values of the

> reduced glutathione in the plasma must be considered equally essential

> (in the lung mucosa and, intracellulary, in the T4 lymph cells of the

> streaming blood)to the laboratory method: Buhl 1989, Herzenberg 1997,

> Nutrall 1998).

>

>

> At the same time, the cysteine level in the plasma must be determined.

> Major deviations from the non-protein-thiol standard value must be

> treated, even in symptom free patients.

>

> As a rule, the organism's need for thiol tends to be underestimated or

> neglected.

>

> After the predominant scenarios in the " thiol-ester-iron world " one of

> the essential conditions for the origin of life in the prebiotic

> world, before the creation of cellular organisms, was sulfur's

> capacity for generating bonds and exchanges between protons of the

> sulfur-hydrogen groups by " weak interactions " , (De Duve 1991).

>

>

>

> Seawater contains naturally an elevated sulfur concentration, but for

> the terrestric life forms exists a consistent danger of latent of

> non-protein thiols and sulfates deficiency. Both are indispensable,

> because they are responsible for the regulation of the redox

> environment, the functioning of the cell symbiosis in immune and

> non-immune cells and innumerable biosyntheses and biochemical

> reactions (Wrong 1993, Hässig 1999).

>

> The pathognomic symptom of cellular immune deficiency (AIDS) and other

> systemic diseases is lack of cysteine and glutathione. (Herzenberg

> 1997, Dröge 1997 b, 1998, Hässig 1998 d, Kremer 1999).

>

>

>

> In symptom-free and symptomatic patients lack of Thiol must be

> compensated in strict and individually adjusted doses.

>

> For an intact cell symbioses " semiconductor barriers " of

> redox-sensitive gene expression must be modulated in a sustainable and

> enduring manner by the redox potential which for retuning enzyme

> activities depends on the glutathione system .

>

> Since the stimulation of the neo-synthesis of glutathione is, due to

> the redox-dependent enzyme synthesis not of itself warranted, for 2 to

> 4 weeks at the beginning of the biological-compensatory therapy at

> least 2 grams of glutathione and 5 to 10 grams of N-acetyle-cysteine

> must be orally administered per day simultaneously.

>

> As a protection against opportunistic pathogens the glutathione

> concentration especially in the mucous membranes, tends to be much

> higher than in the blood plasma (for example, the lung mucous membrane

> liquid contains about 150 to 200 micromoles of glutathione, the blood

> plasma less than 5 micromoles).

>

> An important condition factor for cellular immune deficiency against

> the pneumocystis carinii fungi (which are the pathogens of the most

> common AIDS indicator disease, PCP in the lung) is a lack of

> glutathione in the lung secretion layer.

>

> In case of distinctive resorption dysfunction caused by infectious and

> non-infectuous alterations of the intestinal mucosa, doses of

> glutathione and N-acetyl-cysteine correspondingly reduced can be

> administered I.V.

>

>

>

> After the compensation of the intracellular and the plasma levels in

> the thiol pool and the glutathione concentration in the lung and the

> intestinal mucous membrane liquids, cysteine treatment should be

> continued for another six months with a daily dosage of 5 to 10 grams

> of N-acetyl-cysteine.

>

> Cysteine and methionin, the later is converted in the liver to

> cysteine, can be taken in addition as part of daily nutrition. It is

> contained in low fat curd cheese and other native organic dairy

> products (Bounous 1993).

>

> Due to the deficit of convertible protons, thiol deficiency causes a

> glutamine decrease with exaggerated protein reduction in the skeletal

> muscles (loss of body weight, wasting syndrome). The oral intake of up

> to 40 grams/day of high dosage glutamine can retune the synergic

> effect between glutamine and cysteine levels for the helper T cells

> maturation (Shabert 1999).

>

>

>

> Simultaneously this effect improves the regeneration of intestinal and

> lung mucous membranes, energy metabolism of the cell symbioses and

> acid-base balancing.

>

> The glutamine facilitates detoxification activity in the liver via the

> glutathione system; it slows down the urea production due to decrease

> in the arginine splitting in urea and ornithine.

>

> If in case of a clear arginine deficit and the resulting lack of NO

> gas production (as part of pre-AIDS and AIDS), the thiol and glutamine

> balance is complimented by doses of up to 30 grams of arginine per day

> and up to 2% of the caloric intake respectively. By this the cellular

> immune performance (T4 help cells, natural killer cells, neutrophilic

> granulocytes) can be augmented significantly (Barbul1990, Bower 1990).

>

>

>

> Synergistic adjustment of the dysregulation of amino acids cysteine,

> glutamine and arginine can be achieved in the case of massive immune

> cell deficiency, forced aerobic glykolysis, malignant cell

> transformation and cell degeneration as well as a pronounced wasting

> syndrome, by using small intestinal probes or, if necessary, by

> parenteral infusion solutions. In critical cases of disease,

> glutathione can be administered I.V.

>

> Highly dosed compensation for thiol deficiency and amino acid

> dysregulation must be seen as the basic therapy of the redox

> environment and of a detoxication performance. These are providing the

> organism with much needed and natural surviving resources to

> facilitate its self-regulation. Therapy success must be continuously

> supervised by laboratory checks adapted to individual requirements,

> since the N-acetyl-cysteine is lifting glutamine and arginine levels

> in the plasma (Dröge 1997 a).

>

>

>

> In case of pre-AIDS or AIDS a rigorously administered compensatory

> therapy during a well-monitored treatment phase produces, compared to

> the counterproductive prescription of chemotherapeutic agents (AZT

> etc., cocktail therapy, HAART) and a permanent prophylaxis with

> chemo-antibiotics (Bactrim etc.). better and more cost effective

> results. Chemotherapeutic agents may bring short time results, but

> also produce symptom aggravation.

>

> Should because of acute opportunistic infections a chemo-antibiotic

> (Bactrim etc.) be administered for a short time, it is just then very

> important to administer a consequently metered compensation of the

> thiol deficiency.

>

>

>

> This important compensatory therapy can be effectively supported by a

> set of specific regulatory means during the symptom free phase of the

> acquired immune deficiency as well as in the phase of systemic

> secondary diseases.

>

> Hepatitis is often evident in members of pre-AIDS and AIDS risk

> groups, i.e. promiscuous homosexuals, I.V. drug users and recipients

> of highly contaminated stored blood (Hässig 1996 b, 1998 e). This

> calls for additional liver protection to bring relief to the

> glutathione system and phase-II detox enzymes (Wilkinson 1997).

>

>

>

> In contrast to the phase-I enzymes, which generate reactive

> electrophiles (electron consuming substances) and activate

> carcinogens, phase-II enzymes inhibit electrophile bonds and turn them

> into water soluble excretable substances 'Oltipraz' , is a synthetic

> agent proved highly effective. It was originally designed as an

> anthelmintic against schistosoma, which trigger a type-2 cytokine

> dominance (Lucey 1996), analogical to the earlier stadia of the

> acquired immune deficiency.

>

> 'Oltipraz' is a sulphur-containing dithiolthione. In general it

> activates the enzyme family of glutathione-S-transferases. It exerts a

> protective function in the liver and in many other cell systems,

> especially the intestinal mucous membrane. Beside the protective

> effect against opportunistic germs and endoparasites the agent has

> been proven antiviral and anticancerogenic effects (overview in:

> Wilkinson 1997).

>

> These findings are significant especially after prior prooxidative

> damage caused by mitochondrial cell symbioses through AZT etc. and

> permanent prophylaxis with 'Bactrim. ''Oltipraz' is equally efficient

> in the activation of the detoxication enzymes in the helper T cells

> (Gupta 1995). Because 'Oltipraz' causes sustainable and

> side-effect-poor triggering of the phase-II detoxication enzymes, for

> this 125 to 250 milligrams/m2 for 12 weeks is an adequate dosage.

>

>

>

> Among the natural substances, sulfureous isothione-cyanates provide

> good effective protection by triggering the variegated phase-II

> detoxication enzymes (overview: Hecht 1995). These thiocyanates are

> inherent in vegetables like garlic, onions, broccoli and other cabbage

> species. The other important family of natural liver protecting agents

> are polyphenols. Animal and human organisms are not able to synthesize

> aromatic bonds with benzene rings. Polyphenols must therefore be taken

> with nutrition like algae or other plants so polyphenols work

> similarly to vitamins (Hässig 1997 c).

>

>

>

> The redox-cycling between the glutathione system and the polyphenolic

> substances is crucial for the balancing of the redox environment and

> the detoxication performance by the polyphenols, as well as the

> triggering of the phase-II detoxication enzymes and the inhibition of

> the phase-I enzymes respectively.

>

>

>

> Essentially polyphenols assist enzymes cooperating with reduced and

> oxidised glutathione, glutathione-peroxidase, glutathione-reductase,

> glutathione-S-transferases, katalase, NAD(P)H-quinone-oxidase, and

> they inhibit the enzymes of the cytochrome P450 family (overview:

> Wilkinson 1997).

>

> Antioxidative protection of cell symbioses of liver cells and other

> cell systems including the immune cells by polyphenols is of

> particular importance in the highly acute AIDS state, if, due to the

> failure of the cytotoxic NO-gas producing TH1 helper cells,

> intracellular opportunists can proliferate without inhibition.

>

>

>

> In this precarious situation, type-2 cytokine production is amplified

> on one hand, but on the other hand non-specific immune reaction of the

> phagocytes (macrophages) and the microglia cells in the brain are

> overactivated by the modulation of proinflammatory cytokines

> (interleukin-12, interleukin-1, tumour necrosis factor alpha and

> others, inflammation mediators and nitrogenic and oxidative radicals).

>

>

>

> The elevated quantity of neopterine (as a folic acid metabolism

> product) and the beta-2 protein in the circulating blood are indirect

> markers for an overactivation of the proinflammatory cytokine activity

> of the unspecific immune cells with a simultaneous suppression of the

> cytotoxic NO-gas production of the specific immune cells (AIDS

> full-blown clinical pattern)(Mauri 1990, Odeh 1990, Fuchs 1990,

> Harison 1990, Matsuyama 1991, Krwon 1991, Hässig 1993, Valdez 1997).

>

> Consequently, well balanced cell protecting backlash fails and the

> simultaneous cell toxic overregulations (prevalence of interleukin-12

> compared to type2-cytokine interleukin-10) incapacitate the feedback

> functions. In the case of a thiole deficiency and a too high

> consumption of other antioxidants, the redox-compensation collapses in

> the competing cytokine chaos (Cossarizza 1995).

>

>

>

> The clinical studies concerning polyphenols during the last years have

> mainly been concentrating on ellagic acid. Polyphenols are contained

> in green tea, curcumine, silymarine and others (overview: Stonder

> 1995, Conney 1997, Wilkinson 1997, Zhao 1999, Plummer 1999).

>

> Another possibility is the galenic combination of glutathione with

> polyphenolic anthocyans (Recancostat, Ohlenschläger 1994) and with the

> ginkgo biloba polyphenol (S-acetyle-glutathione, SAG) respectively.

> Liver protection in the case of chronic hepatitis B through

> polyphenolic complexion phytotherapeutic 'Padma 28', produced after

> traditional recipe of Tibetan medicine in Switzerland (PADMA AG,

> Schwerzenbach), containing 20 herbal flavonoids and tannins, has

> proven reliable (Brzosko 1992, Liang 1992, Hässig 1997).

>

>

>

> By reinforcing the supply of glucuronic acid liver cell symbioses can

> additionally be relieved. Glucuronic acid plays an equally important

> role as a phase-II regulator of prooxidative and carcinogen-activating

> foreign agents in the liver and which acts to transform toxins into

> secretable substances.

>

> Kombucha, the organic product from ancient china, containing a

> symbiosis of fungi and specific bacteria is a natural source of

> glucuronic acid, and additionally beside the high concentration of

> glucuronic acid contains vitamin B compounds and antibiotic substances.

>

> Kombucha can be made at home ( 1992).

>

>

>

> The progression of the prostaglandin synthesis under the influence of

> the type2-cytokine dominance is characteristically in the case of

> pre-AIDS or AIDS, part of the type2-counterreaction. This progression

> can be countermodulated therapeutically as well and preventively.

> Elevated quantities of PGE2 inhibit, like the type2-cytokines, the

> synthesis of the cytotoxic NO gas and thus enhance opportunistic

> infections.

>

> The prostaglandins are products of the arachoidonic acid, an essential

> fatty acid.

>

> Arachoidonic acid is enzymatically metabolized into prostaglandin

> within the cells plasma membrane by the enzyme cyclooxigenase (COX).

>

>

>

> In the case of AIDS, cancer and other systemic diseases, the COX-2

> isoform appears elevated. COX-2 increases the PGE2 production. It also

> raises the type-2 cytokine interleukin-6 production, which can trigger

> wasting syndrome (Hack 1996).

>

> Symptomatic for all systemic diseases like AIDS and cancer wasting

> syndrome can be influenced by the selective inhibition of the COX-2

> (O'Hara 1998).

>

>

>

> PGE2 is enzymatically generated by COX-2. In the same sense as growth

> factor TGF-Beta, it activates the generating of polyamines from the

> arginine product ornithine. Therefore, the blockade of COX-2 through

> medication also inhibits tumour growth, reduces wasting syndrome and

> improves the TH1-TH2 balance of the cellular immunity (Subbaramiaiah

> 1997. Huang 1998, 1999, Lipsky 1999a, 1999b, Sawaoka 1999,

> Golden 1999, Masferrer 2000, Kune 2000, Prescott 2000, Reddy 2000,

> Hiashi 2000, Stolina 2000).

>

>

>

> In the case of symptom free patients with a weak or an anergic TH1

> immune cells population, prostaglandin modulation through essential

> fatty acids is a better option for treatment.

>

> In animal testing TH1 helper cells population stimulability in the

> DTH skin reaction test was inhibited, when 15 % of the intake of

> calories consisted of linolenic acid, but not with the same quantity

> of fish oil with its high content of omega-3 fatty acid ( 1990).

>

> As cold-water fish can supply their needs of essential fatty acids by

> eating sea microalgae, patients can cover their requirement of

> essential fatty acids for prostaglandin modulation by the nutritional

> intake of contamination free microalgae in powder or in tablet form

> (e.g. chlorella vulgaris (producer: Ökologische Produkte Altmark GmbH,

> Köthen).

>

>

>

> It is indeed necessary to ingest a couple of grams per day for several

> weeks in order to stimulate immune cell reaction and inhibiting tumour

> creation. The effect of the mitochondrial cell symbiosis protection is

> improved by the simultaneous substitution with cysteine, glutamine,

> arginine and RNA (Bower 1990, Cossarizza 1995, Chuntraskaul 1998,

> Gianotti 1999).

>

>

>

> The low or high fluidity of the cell symbioses' micro-gaia environment

> of as the fluidity of the cell membranes reflect the kind and the

> composition of the multi-unsaturated fatty acids (Bower 1990,

> Fernandes 1998, Simonopoulos 1999, Zelenuich-Jaquotte 2000).

>

> The interaction between the NO and other derivates synthesis and the

> prostaglandin PG E2, which is synthesized from the arachidon essential

> fatty acid, is to a minor degree antagonistic (overview: Lindoln 1997,

> Minghetti 1998).

>

>

>

> This interaction is of vital importance for the prevention and therapy

> of type2-counter-regulations of cell symbioses (systemic diseases)

> including the type1-cytokine-type2-cytokine switch (cellular TH1

> immune deficiency, Pre-AIDS) combined with proinflammatory macrophage

> overactivation (opportunistic infections, AIDS full-blown clinical

> pattern).

>

> It is possible to counter-regulate massive regressions of the cell

> symbioses by type omega-3 multi-unsaturated fatty acids and its

> derivates (Velerod 1997, Imoberdorfr 1997, Gogos 1998, Albert 1998,

> Ogilvie 1998, De Langeril 1998, Tashiro 1998, Rose 1999, Bougnoux

> 1999, Burns 1999, Bartsch 1999, Biasco 1999).

>

>

>

> Using micro nutrients (vitamins, minerals and oligo-elements) must be

> considered in a differentiated way when used as part of a

> biological-compensatory and regulation therapy and prevention of

> Pre-AIDS and AIDS as well as for other systemic diseases.

>

>

>

> " Vitamin E, in combination with vitamin C, is nowadays worldwide the

> antioxidant standard treatment. In " The antioxidant supplement myth " ,

> Herbert critically analyzes this proceeding (Herbert 1994). He

> coherently demonstrates that it's effects are disadvantageous, because

> pharmacological dosages of a single polyphenol, like for example

> vitamin E, in combination with vitamin C and beta-carotene, possibly

> can have some positive, but may in many cases show ill effects,

> depending on the receptor's iron state.

>

> As redox compounds their addition demonstrate both prooxidative and

> antioxidative effects, therefore treatment can be summarized as:

> " (Micro nutrients) supplement can help some consumers, harm others,

> but for most, they don't show any effect whatsoever. "

>

> It has been demonstrated, that vitamin C (ascorbic acid), in the

> presence of redox active transition metals like iron (FE) or copper

> (CU), can act as a prooxidans and so, by the so-called Fenton

> reaction, help to develop highly reactive hydroxide radicals (Fenton

> 1894, Halliwell 1993, Cottier 1995).

>

> The synthesis of hydrogen peroxide (H_2 O_2 ) occurs through a slow

> pH-dependent dismutation of superoxide radicals.

>

> Note: As chelators of free metals tannins can contribute useful

> services in this situation.

>

> Herbert's critical statement has been extensively affirmed by the

> studies of Kim et al., who could not find any life extension effect

> through use of isolated and unbalanced vitamins and mineral nutrition

> supplements.

>

> They identify the annual expenditure of 3.3 billions $ for nutrition

> supplements as a virtually useless augmentation of the health care

> costs (Kim 1993).

>

> " In conclusion, we would like to state: a sufficient nutritive supply

> of a natural mixture of tannins and flavonoids is indispensable for a

> reliable and side-effect free antioxidative effect " (Hässig 1997c).

>

>

>

> Vitamin E and vitamin C generate radical chain reactions as

> intermediate states, which must be compensated for by the glutathione

> system (Ohlenschläger 1994), therefore a given thiol deficiency can be

> aggravated by the intake of a high dosages of those vitamins.

>

> Micro nutrient requirements, in the case of Pre-AIDS and AIDS, should

> be evaluated in the context of the precise regulation of a rigorous

> biological-compensatory and regulation therapy, because deficits of

> several micro nutrients depend on the redox state, the mitochondrial

> activity, the cytokine balance, the existence of a wasting syndrome,

> any given resorption dysfunction, severe diarrhoea, toxic and

> infectious stress-factors, alloantigen overcharge, chemotherapeutic

> agents, chemo antibiotics, antiparasitics, fungistats, virustatics

> etc, excessive alcohol, drug or cigarettes usage and many other

> factors. Uncontrolled self-medication does not make much sense and can

> in some cases even be dangerous.

>

>

>

> An overview study with ambulatory Pre-AIDS and AIDS patients in

> relatively good health without a clinically definable wasting syndrome

> or heavy diarrhoea quantified:

>

> " Vitamin A and complete carotene, vitamins C, E, B_6 , B_12 , folic

> acid, thiamine, niacine, biotine, riboflavin, pantothenic acid, free

> choline and choline total, carnitine, biopterine, inositole, copper,

> zinc, selenium, magnesium and glutathione.

>

> The results of the study confirm a reduction in the circulating

> concentrations of glutathione and relatively often lower serum

> concentration for magnesium, complete carotene and complete choline

> plus increased niacine levels. The remaining values were in normal

> range and lower for a minority of the tested persons respectively,

> sometimes with self-medication through vitamins and minerals "

> (Skurnich 1996).

>

>

>

> The general survey of state of the art clinical research on HIV/AIDS

> medication concerning several micro nutrients as influencing factors

> for acquired immune deficiency states (Pre-AIDS and AIDS) display also

> an individual dependency on deficiencies in a holistic context of

> dysfunctional cell symbioses.

>

>

>

> " Singular micro nutrient deficiencies are known for their

> disadvantageous influence on the immune system by lowering cellular

> and humoral immunity and damaging the phagocytosis " (Beisel 1982,

> Klurfeld 1993). PW-HIVs can react particularly sensitively to

> nutrition based deficiency states, which damage the already suppressed

> immune functions. In an earlier study with people infected by HIV we

> found that carotene and ascorbic acid (vitamin C) have been lowered in

> 27% and vitamins E and A in 12% of the patients " (Bogden 1990).

>

> " The serum levels of micro nutrients in HIV positive patients have

> been associated with immune function- and disease stage-markers

> (Fordyce-Baum 1990, Baum 1991, 1992, Semba 1993). The studies

> demonstrate that an abnormal nutritional status at once, goes along

> with and precedes the progress of the HIV disease (Semba 1993, Coodley

> 1993, Tang 1993, Abrams 1993). These studies evaluated the nutrition

> intake or the serum concentration of one or of a few micro nutrients

> in selected patient-cohorts " (Skurnick 1996).

>

> The relevance of the primary influence of micro nutrients on the

> prevention and therapy of cancer has been qualified in relative terms

> compared to the relevance of the redox status, NO- and prostaglandin

> syntheses, the cytokine balance and cell symbioses activity (World

> Cancer Research Fund 1997).

>

>

>

> An additional measuring of the serum ferritine level must be

> considered essential, which in the case of pre-AIDS or AIDS as in all

> proinflammatory stages of macrophage overactivation is evidently

> elevated (Gupta 1986) and plays an important role in all type-II

> counter-reactions (Gherardi 1991, Weinberg 1992, Herbert 1992, Gelman

> 1992, Lacroix 1992, Kiefer 1993). Apart from the compensatory therapy

> of the redox state (Pippard 1989, Hässig 1993), the reinforcement of

> basic tissue has an important function, in view of the regulation of

> balancing iron.

>

>

>

> The extracellular base-tissue, in which all tissues and organs are

> embedded, functions as filter for the cell symbioses' entire

> bioenergetic, substantial, hormonal and sensory input and output.

>

> Among other, base-tissue is composed of a complex network of

> high-sulfate protein molecules (glycosamine glykanes, proteoglykanes),

> which make up the negative redox potential. Re-fetalization of the

> extracellular matrix of the base-tissue into sulphate free hyaline

> acid, as present in early embryonic tissue, is characteristic for many

> carcinomas (Heine 1997).

>

>

>

> For prevention and therapy, the extracellular matrix can be reinforced

> over a regular supply of polyanions, chondroitine sulphate in the form

> of cartilage preparation, of shark cartilage, of microalgae, of

> agar-agar or by eating macroalgae (Hässig 1992). The redox potential

> equalization of the base-tissue is synergically supporting the

> glutathione system and discharges cell symbioses in prooxidative and

> systemic stress stages (Hässig 1992, 1997a, 1998b).

>

> Direct activation of the mitochondrial cell symbioses can be

> stimulated by coenzyme Q10 (Folkers 1986) and L-carnitine (Bremer 1990).

>

>

>

> Coenzyme Q10 plays an important role in the electron transfer in the

> mitochondria's respiration chain.

>

> In symptom free so-called HIV positives, a Q10 deficit is already

> traceable and will be progressively so in aggravating pre-AIDS and AIDS.

>

> Toxic stress-factors and prooxidative medication (AZT etc., Bactrime

> etc.) are decisive factors in leading to mitochondrial respiration

> chain dysfunction and secondary defects in the mitochondrial DNS.

>

> Q10 improves the cell symbioses performance in immune cells and

> non-immune cells to be administered in a daily dosage of 200

> milligrams for a several months without detectable side effects to be

> expected (overview: Folkers 1988).

>

>

>

> L-carnitine is involved in the infiltration of long-chained fatty

> acids (triglycerids) for the oxidation inside the mitochondria.

> L-carnitine deficits increases the glucose metabolism and

> facilitates a switch to aerobic glykolysis (Warburg phenomenon). The

> disturbance in the triglyceride transport causes lipid accumulation as

> often seen under the treatment with HAART and protease inhibitors

> (Brinkmann 1999). Pre-AIDS and AIDS must be seen as systemic

> dysfunctions of the lipometabolism and of the lipid composition of the

> T-lymphocytes ,in context with a the L-carnitine deficit (De Simone 1991).

>

>

>

> Administrating high dosages of L-carnitine (6 grams per day for two

> weeks) has improved T-helper cells proliferation, lowered the

> triglyceride serum level and decreased the circulating beta-2

> microglobuline and the alpha tumour necrosis factor serum values as

> indicators for macrophages overactivating in patients with AIDS and

> patients tested HIV positive. It seems also that L-carnitine

> stabilizes the cytokine balance by ameliorating the mitochondria

> performance (overview: De Simone 1993).

>

>

>

> Decreased mitochondria performance as long-term chemo consequences,

> caused by mitochondria DNA damage after the intake of AZT etc. and

> Bactrime etc. can additionally be compensated for by daily dose of

> orally 600mg lipoic acid (alpha-lipoic acid) plus 300mg thiamine

> (vitamin B_1 ) for a month or longer (alternatively also intravenously

> in the same dose). Alpha liponic acid is especially a good treatment

> for liver protection.

>

>

>

> Systematic mitochondria activation is of particular significance to

> patients who - so called - tested HIV positive, but equally for cancer

> patients threatened with multiple organ failure (myocardial

> infarction, sepsis, cerebral infarction, hepatic coma, myopathy).

>

> The cytokine balance and resulting the equilibrium between

> cell-mediated and antibody supported immunity interacts, like all

> organ systems, with the sensory and hormonally controlled stress system.

>

>

>

> The retroactive hormonal stress axis between the hypothalamus, the

> hypophysis and the adrenal cortex modulates the cytokine profiles via

> an equilibrium between cortisol and DHEA-S

> (dehydroepiandrosterone-sulphate),both generated in the adrenal cortex.

>

> The final cortisol synthesis takes place in the mitochondrial

> cell-symbionts of the adrenal cortex cells (Tyler 1992). Consequently

> disturbance and damage of these cells can favour grave psychosomatic

> stress diseases and systemic diseases like AIDS, cancer and many other

> symptoms.

>

> During states of high stress, the synthesis and the release of

> cortisol increases when compared to the DHEA-S level.

>

> This causes cytokine synthesis inhibition through cortisol interaction

> with transcription factors (Brattsand 1996).

>

>

>

> Persistent cortisol increase facilitates antibody supported immune

> response and weakens cellular immune reaction.

>

> By inhibition of the type-1 cytokine pattern, under strong stress

> stimulation of the macrophages through antigens and toxins, the

> release of nitrogenic and oxygenic radicals and of the inflammation

> mediators interleukin-1 and tumour necrosis factor-alpha can be

> increased within the macrophages.

>

> As direct scope for quantification of macrophage-activation through

> inflammation can serve the neopterine and ferritine level and as

> indirect measurands as for example the C-reactive protein can serve

> as much as indication of acute phase reactions (Hennebold 1994, Hässig

> 1997d, 1998b).

>

>

>

> If due to a cortisol-DHEA-S ratio Type1(TH1) cytokine pattern can

> shift to type2 (TH2) cytokine dominance increase , this means that in

> reverse, a moderation of stress-caused hypercortisolism amplifies

> DHEA-S effect on the type1 cytokine synthesis.

>

> Therefore an amelioration of the cortisol/DHEA-S ratio in favour of

> the DHEA-S can improve cellular immunity by activating type2 cytokine

> interleukin-2.

>

>

>

>

>

>

>

> There is indeed a direct correlation between the T4 helper cells and

> the cortisol level and the level of the sulphated DHEA-S (the

> predominantly synthesized form) respectively.

>

> The occurrence of acquired cellular immune failure syndrome is

> associated with an increasing DHEA-S deficite (Biglierei 1988, Raffi

> 1991, Mulder 1992, Christeff 1996, Ferrando 1999). With AIDS-patients

> however the 24 hours cortisol level seems elevated (Vilette 1990).

>

> These findings resulted in the hypothesis that DHEA-S substitution

> (DHEA-S as an anti-cortisol hormone) could enhance cellular immunity

> for the prevention and therapy of opportunistic infections in the case

> of pronounced pre-AIDS and AIDS (Frissen 1990, Wisniewski 1993).

>

>

>

> The DHEA-S level as counterbalance to the ACTH cortisol system is of

> vital importance, not only for cytokine controlled functions of the

> immune cells cell symbioses, but also for other cell systems (

> 1985, Ebeling 1994, Lavallee 1996).

>

> DHEA-S as a precursor molecule for sexual hormones, and DHEA-S

> dysregulation are both co-determining factors in the case of tumours

> in hormone dependent organs such as the mammary gland or the prostate

> as much as of tumours in other organs (Vermeulen 1986, Heinonen 1987,

> Barett-Connor 1990, Stahl 1992, Le Bail 1998, Lissonie 1998, Svec

> 1998, Eaton 1999).

>

>

>

> Hypercortisolism moderation and direct type2 cytokine stimulation via

> DHEA-S can in many cases be supported by nutritive measures.

>

> Among others the increase of the extracellular content of glycosamine

> glycanes (Heparine, Heparinoids) is useful. They reduce the calcium

> ions influx into the inner cell and inhibit cortisol bonding on the

> intracellular receptors.

>

> This can be achieved through an intake of cartilage extracts

> (chondroitine sulfate) or of agar from sea algae (Hässig 1993, 1998b).

>

>

>

> Simultaneously the proinflammatory overactivation of macrophages in

> typ1-type2 cytokine shifts can be repressed by binding surplus NO and

> O_2 radical through intercepting excessive free iron and an increase

> in catabolic proteases generation by using complex phytotherapeutics

> like Padma 28, a Tibetan combination preparation made up of

> polyphenolic flavonoids and tannins (Liang 1992, Hässig 1993, Gebbers

> 1995).

>

> Cortisol moderation and the reactivation of DHEA-S in interaction

> with 'proinflammatory macrophages stimulation inhibition' is important

> because in addition macrophages through their phagocytosis performance

> capacity represent a preferred reservoir for intracellular

> opportunistic pathogens (Rubin 1988, Meltzer 1992).

>

>

>

> Sooner or later the counteraction to a strong and long-lasting

> nitrosative prooxidative and systemic stress effect with the

> consequence of a elevated cortisol/DHEA-S ratio, failure of cellular

> immunity and of the cytotoxic NO gas defence through a cytokine type2

> switch and proinflammatory mobilisation of opportunistic residents in

> the macrophages (fungi like pneumocystis, candida, histoplasms,

> cryptococci, parasites and toxoplasms, bacteria like mycobacteria,

> listeria, legionella and chlamydia and many actually existing viruses

> (in contrast to the so-called Hi viruses)) must lead to clinical

> full-blown AIDS, if the primary stress factors can not be minimized,

> the proton demand deficiencies are not balanced and the

> dysregulation of the cell symbioses is aggravated additionally through

> the use of chemotactic weapons.

>

>

>

> With full-blown AIDS this results in a crucial antagonism between the

> behaviour of the non-specific immune response of the macrophages and

> the specific immune respone of T4 helper immunecells:

>

> The cortisol brake for the 'tumour necrosis factor's biosynthesis' is

> disgarded in the macrophages by the activation of interferon-gamma

> under strong or/and long-standing stress stimulation (Luedke 1990) and

> the cortisol/DHEA-S ratio is thus inhibited in favor of the later

> through an inflammatory cytokine influence (Hennebold 1994) The T-4

> helpercells remain inhibited under influence of cortisol and

> synthesize after receiving signals from the antigen presenting

> dendritic cells, which are poor in reduced glutathione, predominantly

> type2 cytokines ( 1998).

>

> They inhibit the cytotoxic NO gas synthesis, contrary to the

> macrophages (loss of helper TH1 cell functions) and stimulate instead

> the antibody production (overview: Mosmann 1996, Lucey 1996, Abbas

> 1996, Hässig 1996d, Lincoln 1997). This results in the increase of the

> cortisol/DHEA-S ratio on the cost of DHEA-S in the T4-immunecells

> (Wisniewski 1993, Christeff 1996, Ferrando 1999).

>

> From this antagonism of unspecific inflammatory events combined with

> the mobilisation of opportunistic pathogens on one hand and the loss

> of the specific TH1 gas production against intracellular opportunists

> on the other hand results the contradictory clinical symptoms of

> manifest AIDS.

>

> The prooxidative, glutathione consuming and mitochondria-toxic

> chemotherapy with AZT etc. and the continuous prophylaxis with Bactrim

> etc. are not able to control the intercompeting cytokine chaos

> resulting from unspecific immune overactivations within the

> macrophages (type-I overregulation: among others: type1 cytokine

> interleukin-12 antagonistic against interleukin-10; tumor necrosis

> factor alpha increased, type 1 cytokine interferon gamma increased;

> NO-and oxygen-radicals inclusive toxic hydroxyl groups enhanced) and

> coincidentally inactivation of the specific TH1 immune respone(Type

> II-counter-regulation: among others: type 2 cytokine, Interleukin 10

> antagonistic against Interleukin 12; in the case of wasting syndrome

> type2 cytokine interleukin 6 enhanced; in the case of tumor cells TGF

> beta increased; NO-and O2-production inhibited).

>

>

>

> The most efficient option is compensating the thiol deficiency,

> empowering cysteine to slow down the toxic cell effects of the tumour

> necrosis factor within the overactivated macrophages and improve

> glutathione neosynthesis (Cossarizza 1995).

>

> The preventive and therapeutic aim must be to balance the redox

> environment, to ameliorate the micro-gaia milieu fluidity, to

> reconstruct the cytokine balance and to reduce the concurrence between

> the type-I overregulation of the unspecific immune reaction and

> simultaneously moderate the specific immunity's type-II

> counter-regulation via a synergistic compensation and regulation therapy.

>

>

>

> " Last but not least it is essential to decidedly confront the still

> popular and official doctrine that every HIV-infected person must

> sooner or later enter full blown AIDS and thus inevitably die (Hässig

> 1992b).

>

> To the contrary we should give HIV-infected persons hope that they may

> be spared from falling ill with AIDS, if they learn to adapt their

> lifestyle to the possibilities and limits given by nature. For this,

> dealing with nutrition problems seems to be most adequate. In our

> overview work, which has been published about one year ago,

> " Rethinking AIDS " , we ask, if this could lead to a paradigm shift in

> medicine (Hässig 1992b).

>

> Nowadays, we tend to assume, such a shift will happen. The use of AZT

> and analogous virucidal medication as recommended by the responsible

> authorities, is based on the antibiotics paradigm, which means the

> toxicologic extinction of microbial inflammation germs. By the same

> token man lives in a ongoing symbioses with a whole slew of

> micro-organisms, hence the question is justifiable if it wouldn't be

> more sensible to support the organism's probiotic, physiological

> mechanisms of self-healing " (Hässig 1993).

>

>

>

> The variety of the efficient and non-toxic intervention options

> demonstrates a possible change within medical practice " from

> antibiosis to symbiosis " .

>

> Therefore, it is the prior medical task of MDs to reduce the

> paralizing and destructive fear of death and instead encourage people

> affected by systemic cell dyssymbioses by reinforcing their natural

> will to survive via a clarification of the actual standard of knowledge.

>

>

>

> The most efficient protection against the abuse of a " violent

> medicine " (Albonico 1997) as a modern instrument of terror and fear

> is the rational knowledge, that any kind of risk for, and any targeted

> attack on the cell symbioses of immune cells and non-immune cells will

> find a constitutional evolutionary biological respond.

>

>

>

> An imagined " HIV retrovirus " would not make an exeption, if it would

> exist.

>

> The clinically monitored symptoms in the case of Pre-AIDS and AIDS

> could, if a biologically active " HIV causative agent " actually was the

> cause of the disease, also could be caused by the disturbance of the

> redox balance, cell symbiosis damage and by the shifting within the

> micro-gaia environment.

>

> The preventive and therapeutical consequences for the inactivation of

> such a " HIV retrovirus " (not proved in biological reality) would be

> principally the same as for all other prooxidative exposure factors.

>

>

>

> Irrespective of the kind of the expositions these basic consequences

> are universally valid, whether, they be of a toxic, pharmacotoxic,

> traumatic, inflammatory, infectious, nutritive, radiative,

> alloantigenic, psychic or sundry nature. People with a strong redox

> sensitive disposition must be treated in every case with the same

> manner to avoid exposition risks and orientate their nutrition

> according to their blood group as a chiffre for genetically disposed

> polymorphism of the enzyme systems (D'Amato 2000).

>

>

>

> The vital importance of a synergy between a conscious compensatory and

> regulatory therapy is deduced from the logic of natural laws

> pertaining to the co-evolution between microbes and man, the

> processing of toxins and other bioactive stress factors, including the

> consequences of an underfeeding or a malnutrition.

>

> The profound change of the rational knowledge of the sciences of

> nature towards healing points from antibiosis (greek anti for against,

> bios for life) to symbiosis (greek sym for with, together).

>

> The predictable end of the lethal hunt for the virus and of one sided

> aggressive cancer expunging means represents at the same time for both

> concerned as for medical therapists as for general population a

> self-critical act of relief from the staging of collective and

> exploitable terrorism of fear.

>

>

>

>

>

>

>

>

>